ArticlePain2026
The prokineticin system and glia cells as pharmacological targets to control neuroinflammation and to relieve pain in a murine model of Fabry-Anderson disease.
Article in Pain, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Reduced Neuroinflammation and Pain with a Functional Sourdough Bread Enriched with Legumes and Ancient Cereals in a Mouse Model of LPS-Induced Inflammation.International journal of molecular sciences · 2026Article
- Astrocytes in Neuropathic Pain: Mechanistic and Global Insights.Pain research & management · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
abstractNeuropathic pain is a major symptom of Fabry-Anderson disease (FD). It develops in childhood, is life-lasting, and resists current therapies; finding new therapeutic strategies is urgently needed. We demonstrate that neuroinflammation control effectively relieves FD pain. We used 2 pharmacological approaches: the microglial inhibitor minocycline and the block of the activity of the chemokine prokineticin-2 with the specific receptor antagonist PC1 (patented compound 1). Ten- and 25-week-old male GLA-/- mice (the FD murine model) were used. These mice were characterized by mechanical allodynia, thermal hyperalgesia, hyposensitivity to cold stimuli, and abdominal pain. Two weeks of treatment with minocycline or PC1 successfully counteracted sensory alterations. A significant inflammatory state, characterized by high levels of prokineticin-2 and proinflammatory cytokines, was present in the FD gut. The sciatic nerve showed initial severe neuroinflammation that attenuated over time. In dorsal root ganglia, neuroinflammation was severe and persistent with prokineticin-2, proinflammatory cytokines, ionized calcium-binding adapter molecule 1, and glial fibrillary acidic protein overexpression; histone demethylases KDM6A and B were also upregulated. We highlighted neuroinflammation in the spinal cord that increased over time. Treatment with minocycline or PC1 significantly counteracted inflammation and neuroinflammation, reducing prokineticin-2 and proinflammatory cytokines levels and increasing anti-inflammatory factor PPARγ expression. Both treatments prevented the onset of micro- and astrogliosis in the spinal cord. We underline the role of neuroinflammation and microglia in FD pain and suggest that treatments that control the activity of the prokineticin system, glial activation, and the production of proinflammatory cytokines and increase anti-inflammatory mediators have a therapeutic effect on pain in FD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.